The hypothesis upon which this proposal rests is that the reduced fertility in PCOS women with LH hypersecretion and hyperinsulinemia is caused, in part, by impaired meiotic and developmental competence of oocytes incurred during oocyte development and/or maturation, and that these impairments are associated with abnormal follicular fluid concentrations of androgens and inhibins. Prenatally androgenized female rhesus monkeys will serve as a model for PCOS because they demonstrate LH hypersecretion, hyperandrogenism, hyperinsulinemia and anovulation. The Specific Aims of the proposal are to determine whether meiotic and developmental competence are impaired in oocytes collected from ovulatory and anovulatory prenatally androgenized versus control ovulatory adult female rhesus monkeys, whether oocyte impairment is related to aberrant follicular fluid or circulating hormone concentrations during folliculogenesis, and whether in vitro maturation (IVM) of oocytes can improve their meiotic and developmental capacity. In vitro fertilization, (IVM) of oocytes and embryo culture techniques will assess the impact of LH hypersecretion and hyperinsulinemia in vivo on the meiotic and developmental competence of oocytes in vitro. This proposal also will identify the role of inhibins as markers of follicle maturity and oocyte competency and insulin as a marker of follicular recruitment during ovarian stimulation. The experimental data will be used for future studies that will investigate how polypeptide growth/differentiation factors of granulosa cell origin participate in the regulation of ovarian function.